PubMed · 4612659
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G H Glaser. 1974. Brain dysfunction in uremia.. https://pubmed.ncbi.nlm.nih.gov/4612659/
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Early transplant dysfunction and failure because of immunological and nonimmunological factors still presents a significant clinical problem for transplant recipients. A critical unmet need is the noninvasive detection and prediction of immune injury such that acute injury can be reversed by proactive immunosuppression titration. In this study, we used iTRAQ -based proteomic discovery and targeted ELISA validation to discover and validate candidate urine protein biomarkers from 262 renal allograft recipients with biopsy-confirmed allograft injury. Urine samples were randomly split into a training set of 108 patients and an independent validation set of 154 patients, which comprised the clinical biopsy-confirmed phenotypes of acute rejection (AR) (n = 74), stable graft (STA) (n = 74), chronic allograft injury (CAI) (n = 58), BK virus nephritis (BKVN) (n = 38), nephrotic syndrome (NS) (n = 8), and healthy, normal control (HC) (n = 10). A total of 389 proteins were measured that displayed differential abundances across urine specimens of the injury types (p < 0.05) with a significant finding that SUMO2 (small ubiquitin-related modifier 2) was identified as a "hub" protein for graft injury irrespective of causation. Sixty-nine urine proteins had differences in abundance (p < 0.01) in AR compared with stable graft, of which 12 proteins were up-regulated in AR with a mean fold increase of 2.8. Nine urine proteins were highly specific for AR because of their significant differences (p < 0.01; fold increase >1.5) from all other transplant categories (HLA class II protein HLA-DRB1, KRT14, HIST1H4B, FGG, ACTB, FGB, FGA, KRT7, DPP4). Increased levels of three of these proteins, fibrinogen beta (FGB; p = 0.04), fibrinogen gamma (FGG; p = 0.03), and HLA DRB1 (p = 0.003) were validated by ELISA in AR using an independent sample set. The fibrinogen proteins further segregated AR from BK virus nephritis (FGB p = 0.03, FGG p = 0.02), a finding that supports the utility of monitoring these urinary proteins for the specific and sensitive noninvasive diagnosis of acute renal allograft rejection.
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BACKGROUND: Few studies have evaluated the association between use of nonsteroidal anti-inflammatory drugs (NSAIDs) and the risk of idiopathic acute renal failure (ARF) in the general population. METHODS: Population-based case-control study among persons in the Canadian province of Saskatchewan who received at least 1 NSAID prescription between January 1, 1982, and December 31, 1986. Health department databases were used for case detection, as the sampling frame for selecting controls (n = 1997), and as the primary source of information on drug use and comorbidity. A total of 306 hospital records were reviewed. Twenty-eight patients who were hospitalized fulfilled the diagnostic criteria for ARF. RESULTS: The incidence rate of hospitalization for ARF among the general population not exposed to NSAIDs was 2 per 100000 person-years. Current exposure to NSAIDs, acetylsalicylic acid and other nephrotoxic drugs, male gender, increasing age, cardiovascular comorbidity, and recent hospitalization for disorders other than renal were found to be independent risk factors for ARF. Current NSAID users had an adjusted odds ratio for ARF of 4.1 (95% confidence interval, 1.5-10.8). The risk of ARF was especially high during the first month of use (odds ratio, 8.5). For prescribed dose, we found that users of high daily doses of NSAIDs experienced an odds ratio of 9.8 for ARF. CONCLUSIONS: In the general population, hospitalizations for ARF were found to be a rare condition. The 4-fold increase in risk associated with NSAID use was dose-dependent and occurred especially during the first month of therapy. Concurrent comedication with other potentially nephrotoxic agents should be prescribed with care, especially in the elderly.